Hypertension and Heart Failure

1. HypertensionandHeart Failure Paul Sutton, MD PhD plsutton@u.washington.edu Medicine 665

2. Goals Case-based approach Epidemiology Associated morbidity and mortality Diagnostic evaluation Risk stratification Treatment Follow-up

3. Hypertension

4. HTN: epidemiology 50 million Americans ?140/90 (70% have stage I HTN) Prevalence increases with age average age at onset: 32 y.o. at age 65: 30% whites, 50% blacks affected Increased risk of stroke, congestive heart failure (CHF) peripheral vascular disease (PVD), coronary artery disease (CAD), atrial fibrillation, renal insufficiency, and death Risk increases steadily for BP > 120/80 Decreased life expectancy of 10-20 years for the average person with HTNDecreased life expectancy of 10-20 years for the average person with HTN

5. Why treat HTN? A little reduction goes a long way A meta-analysis of 14 RCTs showed that decreasing DBP by 5-6 points decreases mortality by 42% over 4-6 years Treatment reduces the risk of stroke, ischemic heart events, CHF, and renal failure Only 59% of patients with HTN are under treatment, and < 1/3 are controlled to ? 140/90

6. Definition of hypertension Simplifies categories But, medicalizes �pre-hypertension� & recommends lifestyle modification, �drugs for compelling indications:� heart failure, post-MI, �high coronary risk�, hx of stroke, chronic kidney disease, diabetesSimplifies categories But, medicalizes �pre-hypertension� & recommends lifestyle modification, �drugs for compelling indications:� heart failure, post-MI, �high coronary risk�, hx of stroke, chronic kidney disease, diabetes

7. Diagnosis 3 visits, unless BP > 180/110 Proper cuff size, arm supported at the level of the heart Use the higher of two arms Repeat after several minutes False positives Cigarettes, caffeine, pain, anxiety Drugs: amphetamines, cocaine, cold remedies, NSAIDs, estrogen, glucocorticoids, TCAs, cyclosporine, licorice, ma huang, ephedra Consider �white coat� hypertension in patients with office-home mismatch (about 25% of patients with mild office HTN) Small cuff will artificially elevate bp.Small cuff will artificially elevate bp.

8. Risk stratification Those at greatest risk derive greatest benefit from treatment Assess for other cardiovascular disease or risk factors Risk stratification influences (a) intensity of intervention and (b) choice of drug

9. History Symptoms (generally asymptomatic) Evaluate for end-organ damage LVH, CAD, CHF, TIA/CVA, PVD, renal insufficiency (Cr > 1.5), albuminuria, retinopathy Other CV risks (heightens risk): cigarette use, lipids, diabetes, obesity, FH of premature coronary disease Lifestyle (potentially modifiable): sodium and fat intake, alcohol, drugs, medications (prescription and OTC/herbal), exercise (inactivity increases risk by 20-50%)

10. Physical Exam Height, weight, appearance (e.g. cushingoid) BMI 25-29 is overweight, >30 is obese Fundi, thyroid exam Cardiovascular exam PMI, S4, S3 Bruits, aneurysms, pulses Extremities cyanosis, edema, wounds, hair Neurological exam

11. Laboratory Evaluation Na, K, BUN, Cr: renal disease, hyperaldosteronism UA: dysmorphic red cells, casts, proteinuria Glucose: diabetes, Cushing�s Cholesterol: risk factor EKG: evaluate for hypertrophy, ischemia Special tests for secondary hypertension: renal artery duplex; renin/aldosterone ratio; 24-hour urinary cortisol; plasma free metanephrine

12. Case 1 A 20 y.o. woman college student is referred to clinic for evaluation for hypertension detected during a sports physical and confirmed at a second visit. Today, she reports intermittent episodes of anxiety, palpitations, and dizziness that she has attributed to stress. PE: BP = 170/102; P = 102 supine. BP = 154/98; P = 118 standing. Thyroid is normal. A faint bruit is heard on auscultation of her abdomen. Labs: Na is 138; K 3.4; BUN 29; Cr 0.7. List possible causes for her hypertension? A colleague suggests starting HCTZ and seeing the patient back in two weeks. Do you agree? Young for primary HTN (although still epidemiologically the leading Dx) Bruit raises possibility of renovascular HTN, most like fibromuscular dysplasia in a young woman (as opposed to renal artery atherosclerosis in an older patient). Also, elevated BUN/Cr Episodic anxiety, orthostasis raise the possibility of pheo Low K raises the possibility of hyperaldosteronism Young for primary HTN (although still epidemiologically the leading Dx) Bruit raises possibility of renovascular HTN, most like fibromuscular dysplasia in a young woman (as opposed to renal artery atherosclerosis in an older patient). Also, elevated BUN/Cr Episodic anxiety, orthostasis raise the possibility of pheo Low K raises the possibility of hyperaldosteronism

13. Resistant/Secondary Hypertension Consider evaluation if: sudden onset, malignant, evidence of end-organ damage, physical findings (e.g., cushingoid), poor response (? 3 drugs, including a diuretic) Only 2-10% of outpatients have secondary causes of hypertension Drugs: EtOH, sympathomimetics, OTCs include NSAIDs & OCPs, pseudophed, Rx include NSAIDs Fibromuscular dysplasia in younger women, atherosclerosis in older patients with risk factors for pvd and/or cad. Coarctation: check bp in lower extremities.Drugs: EtOH, sympathomimetics, OTCs include NSAIDs & OCPs, pseudophed, Rx include NSAIDs Fibromuscular dysplasia in younger women, atherosclerosis in older patients with risk factors for pvd and/or cad. Coarctation: check bp in lower extremities.

14. Causes of resistant HTN From a referral clinicFrom a referral clinic

15. Secondary Hypertension Causes of secondary hypertension Intrinsic renal disease is 0.5-3% Sleep apnea Drugs: recreational, OTC, and prescribed Renovascular: atherosclerosis or fibromuscular dysplasia Endocrine: Cushing�s syndrome, hyperaldosteronism, thyroid disease, acromegaly, hyperparathyroidism Pre-eclampsia Coarctation of the aorta (BP in legs?) Pheochromocytoma Drugs: EtOH, sympathomimetics, OTCs include NSAIDs, OCPs, pseudophed, Rx include NSAIDs Fibromuscular dysplasia in younger women, atherosclerosis in older patients with risk factors for pvd and/or cad. Coarctation: check bp in lower extremities.Drugs: EtOH, sympathomimetics, OTCs include NSAIDs, OCPs, pseudophed, Rx include NSAIDs Fibromuscular dysplasia in younger women, atherosclerosis in older patients with risk factors for pvd and/or cad. Coarctation: check bp in lower extremities.

17. Case 2 A 48 y.o. man who smokes 1 pack of cigarettes per day, drinks 3-4 beers each night, and has Type 2 diabetes treated with metformin, is referred for hypertension. His father had hypertension and died of an MI at 50. His BP remains 158/94 despite atenolol 100 mg qday. Pulse 62. BMI 29. He has an S4, and left carotid and right femoral bruits. The patient reports difficulties paying for his medications. What are his cardiac risks?

18. Case 2 A 48 y.o. man who smokes 1 pack of cigarettes per day, drinks 3-4 beers each night, and has Type 2 diabetes treated with metformin, is referred for hypertension. His father had hypertension and died of an MI at 50. His BP remains 158/94 despite atenolol 100 mg qday. Pulse 62. BMI 29. He has an S4, and left carotid and right femoral bruits. High Risk Stage I Hypertension Cigarettes Type 2 diabetes Family history ? LVH (presence of an S4) Peripheral vascular disease

19. Case 2 A 48 y.o. man who smokes 1 pack of cigarettes per day, drinks 3-4 beers each night, and has Type 2 diabetes treated with metformin, is referred for hypertension. His father had hypertension and died of an MI at 50. His BP remains 192/104 despite atenolol 100 mg qd. Pulse 62. BMI 29. He has an S4, and left carotid and right femoral bruits. Outline a treatment strategy.

20. Case 2 A 48 y.o. man who smokes 1 pack of cigarettes per day, drinks 3-4 beers each night, and has Type 2 diabetes treated with metformin, is referred for hypertension. His father had hypertension and died of an MI at 50. His BP remains 192/104 despite atenolol 100 mg qd. Pulse 62. BMI 29. He has an S4, and left carotid and right femoral bruits. High Risk Stage I HTN Treat today Smoking cessation & other lifestyle modification ACE-inhibitor (or ARB) Thiazide Statin Aspirin

21.  Cigarette cessation! Aerobic exercise Weight loss in obese patients Diet

22. Lifestyle Treatment: Exercise Exercise recommendation 40 minutes of moderate exercise 4-5 days/week Walking >20 minutes to work reduced risk of hypertension in Japanese men by 29%: NNT 26 Walking at work >10,000 steps reduces BP by 10/8

23.  Salt restriction � average dietary NaCl is about 9-12 grams Recommended < 2.4 gm Na (or 6 gm NaCl) � reduce sodium intake by ? � �. Decrease of 2.9 + 1.6 mm Hg; decrease in CV events About 50% of patients are salt sensitive Including most elderly patients Obesity Renal insufficiency

24.  DASH (Dietary Approaches to Stop Hypertension) http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/index.htm 459 patients with Stage I HTN randomized to control diet (low in fruits/vegetables) vs. �DASH diet:� rich in fruits and vegetables, low fat dairy, low in saturated & total fat Avg. blood pressure reduction 5.5/3.0 Sodium restricted follow up study Avg. BP reduction 8.9/4.5

25. Treatment Pearls Blood pressure lowering is more important than the choice of drug Start with a single agent, but adjust regularly; 2 or more drugs are frequently required Recent ALLHAT study supports use of diuretic as 1st agent in patients ? 55 yoa and additional CV risk factors (RCT of 33,357 patients over 5 years) Primary outcome (fatal cardiovascular events or nonfatal MI): no difference among classes Less CHF than CCB (amlodipine) Fewer CV events, stroke, and CHF than ACE-I (lisinopril) Abundant studies demonstrate mortality benefit and reduction in cardiovascular outcomes, principally stroke, with thiazide diuretics.Abundant studies demonstrate mortality benefit and reduction in cardiovascular outcomes, principally stroke, with thiazide diuretics.

26. Treatment Pearls Other agents are acceptable; consider side-effects and cost b-blockers may increase the risk of stroke compared with other antihypertensives ?-blockers help with BPH, but increase risk of CHF If inadequate response, increase dose or add a drug with a complementary mechanism 25-45% of patients >50 yo needed at least 2 agents ~20% needed more than 2 agents Thiazide + ACE I or calcium channel blocker ACE-I + Thiazide or calcium channel blocker ALLHAT included an alpha-blocker arm, stopped early because of the increase in CHF. I use these agents in BPH, but don�t push the dose for antihypertensive effects.ALLHAT included an alpha-blocker arm, stopped early because of the increase in CHF. I use these agents in BPH, but don�t push the dose for antihypertensive effects.

27. Treatment: Special Considerations Diabetes: ACE-Is > ARBs Target < 130/80, ideal < 120/80 Thiazides and ?-blockers increase insulin resistance and lipids, but decrease mortality! The recent UKPDS study in type II diabetes suggests that ACE-Is and ?-blockers confer equivalent benefit Thiazides: Do not exceed 25mg (perhaps an increase in sudden death) Not effective in patients with renal insufficiency (Cr > 2 � 2.5) Important side effects include hyponatremia, hypokalemia, and gout CCBs are a distant 3rd line in patients with diabetes. CCBs are a distant 3rd line in patients with diabetes.

28. Treatment: Special Considerations ?-blockers: b-blockers may increase the risk of stroke compared with other antihypertensives Not currently recommended as 1st line therapy for uncomplicated HTN Ideal choice in patients with angina, arrhythmias, migraine Difficult with asthma (consider ?1-selective), but OK with COPD, diabetes Avoid b-blockers with CCBs that affect conduction (verapamil or diltiazem) Pregnancy: methyldopa, ?-blockers Avoid diuretics & ACE-Is CCBs are a distant 3rd line in patients with diabetes. Race remains controversial � does this concept really have any genetic/pharmacological meaning?? CCBs are a distant 3rd line in patients with diabetes. Race remains controversial � does this concept really have any genetic/pharmacological meaning??

29. Case 3 A 42 year old lawyer comes in for his annual physical exam and his BP is 148/96. He has no family history, does not smoke, total cholesterol was 180 last year. His BMI is 27. He does not get regular exercise. Does he have hypertension? Should he be treated and how?

30. Should you treat mild HTN? Treatment of mild HTN study (TOMHS) 45-69 y.o. patients with DBP<100 Placebo vs. ?-blockers, ?-blockers, CCBs, ACEIs, or thiazides 5.1% decrease in CV events over 4 years no difference in CV outcomes by drug QOL marginally better with thiazides and ?-blockers Start with lifestyle for 6-12 months if low risk Stage 1 (< 160/100 mm Hg) And no CVD or diabetes, no end-organ injury

31. Case 4 A 75 year old woman returns to the clinic for follow-up. Blood pressures were 160-170/70-80 at presentation and are now 140-150/60-70 on amlodipine 5 mg/day. She asks if she can stop her medication because she thinks it�s making her tired and her feet are swelling, making it difficult to wear her best shoes. BP 149/62. P 84. What should you tell her? Change drugs Consider a trial of lifestyle management & off drugs.Change drugs Consider a trial of lifestyle management & off drugs.

32. Should you treat systolic HTN? Systolic hypertension is common: 87% of patients > 50 The SHEP trial showed that treatment to <160/95 decreases CV events (including MI and stroke) ~ 30% HYVET showed antihypertensive Rx reduced all-cause mortality, stroke, & CV events among hypertensive �very elderly� (3895 patients over 80) Lower extremity edema is common with calcium channel blockers Consider thiazide (chlorthalidone or HCTZ) vs. ACE-I

33. Case 5 A 62 y.o. white man presents to the ER with HA, confusion, and blurred vision for 3 days. He has hypertension treated with atenolol, lisinopril, and HCTZ. He has not had fever, chills, and says he takes all his pills (verified by his wife). He has no history of chronic headaches. BP = 230/124; P = 96; T = 36.8 C. You notice bilateral retinal flame hemorrhages, a laterally displaced PMI, and an S4. His neck is supple. Labs: BUN 36, Cr 2.4 (Baseline BUN 22, Cr 1.6). CXR is normal. EKG shows LVH with strain. What is your differential diagnosis? What is your initial management plan?

34. Malignant Hypertension Acute process with end-organ damage: ~1% of patients with HTN. SBP often ? 200, DBP often ? 110. chest pain, EKG changes HA, encephalopathy, papilledema elevated creatinine, proteinuria, hematuria Treatment Hospitalize with arterial monitoring (ICU) Lower DBP by 25 % over 2-6 hours to ~ 100 nitroprusside, labetolol, diazoxide, enalaprilat Avoid short-acting agentsAvoid short-acting agents

35. HTN take home points 25% of Americans have HTN but only a very few have secondary HTN: don�t work everyone up Ideal BP is 120/80 and most patients� blood pressures are not well controlled Lifestyle change is important! Talk to patients about lifestyle. Use motivational strategies. What�s important to them? What do they think about their HTN? Thiazide diuretics are a good first choice: Drug choice is less important than BP achieved ACE-I with diabetes, renal insufficiency, or left ventricular dysfunction B-blockers or CCB with angina or arrhythmia

36. Heart Failure

37. Heart Failure: epidemiology Abnormal cardiac function resulting in inadequate blood supply to maintain normal body functions (arterial underfilling) CAD most common cause, HTN, valvular disease More common as we age: 10% of people >75 yoa have HF 88% of new diagnoses are in patients ? 65 yoa Leading cause of hospitalization in Medicare population 5-year survival: 60% men, 45% women NY class IV 1 year mortality is 50% Death is usually due to ischemic/arrhythmic sudden death or refractory HF 

39. HF: Differential Diagnosis Leading etiologies: IHD 36% Idiopathic 34% HTN 14% Valvular disease 7% Atrial fibrillation 5% Other causes 5% Types of heart failure: Dilated (low output vs. high output) Restrictive (infiltrative) Hypertrophic Constrictive (pericardial) Low output: typical ischemic cardiomyopathy or cardiomyopathy viral/HIV, valvular, EtOH, hypertensive, familial, metabolic High output: hyperthyroidism, AV malformation, wet beriberi, Paget�s, tachyarrythmia, anemia, prolonged infection/fever Restrictive: sarcoidosis, amyloidosis, hemochromatosis Hypertrophic: HOCM, Hypertension, Aortic stenosis Constrictive: post-surgical (pericardial), TB, rheumatologic, malignancy, viral Low output: typical ischemic cardiomyopathy or cardiomyopathy viral/HIV, valvular, EtOH, hypertensive, familial, metabolic High output: hyperthyroidism, AV malformation, wet beriberi, Paget�s, tachyarrythmia, anemia, prolonged infection/fever Restrictive: sarcoidosis, amyloidosis, hemochromatosis Hypertrophic: HOCM, Hypertension, Aortic stenosis Constrictive: post-surgical (pericardial), TB, rheumatologic, malignancy, viral

40. Case 1 A 62 y.o. woman presents to your office concerned about shortness of breath, while walking and when trying to sleep, one month after a non Q-wave MI. She is taking atenolol and isosorbide dinitrate. What is your impression and what physical exam findings would confirm it?

41. Heart Failure: Symptoms Left-Sided DOE (LR 1.3) Orthopnea (LR 2.0) PND Nocturnal cough Nocturnal awakening Palpitations Exertional fatigue Nocturia Hemoptysis Right-sided Abdominal bloating Hiccups Anorexia Weight loss

42. Heart Failure: Signs Left-sided S3 Rales Pleural effusion Altered respiration Displaced/enlarged PMI Murmur Cool extremities Pulsus alternans Right-sided Elevated CVP Sternal lift Peripheral edema Ascites Hepatomegaly Abdominal Jugular Reflux (AJR)

43. Evidence-Based Physical Exam CVP > 8 cm @ bedside: LR 9.0 for volume overload (?LVEDP) Abdominojugular reflux: LR 8.0 for volume overload (?LVEDP) Enlarged or laterally displaced PMI: LR 4.7 � 8.0 for dilated cardiomyopathy (?LVEDV) S3 gallop: LR 3.8-4.1 for depressed ejection fraction

44. Diagnostic Evaluation Basic Electrolytes Cardiac enzymes Lipids EKG CXR Echocardiogram ? BNP (B-type natiuretic peptide) Other Thyroid functions Liver function tests Ferritin Antinuclear antibody HIV SPEP, UPEP (serum and urine protein electrophoresis)

45. Case 2 A 60 year-old man with a history of chronic stable angina develops ankle swelling and increasing shortness of breath during his daily walks. PMH: type 2 DM, hyperlipidemia, quit smoking 5 years ago. He takes metformin, pravastatin, ASA, and prn nitroglycerin. JVP is 10 cm, RRR S1, S2, +S3 without murmurs; AJR is positive; 2+ edema. His EKG shows old Q waves in II, III, and aVF. How will you treat him?

46. HF: general care Low salt diet average American diet = 9 - 12 gm no added salt = 4 gm Exercise Avoid alcohol Self-monitoring: daily weights Discuss medication adherence Check for medication interactions

47. NYHA Functional Class Class I: No limitations of ordinary physical activity; ordinary activity does not produce fatigue, dyspnea, palpitations, or angina Class II: Slight limitation of activity Class III: Marked limitation; minimal activity leads to symptoms Class IV: Symptoms at rest; exacerbation of symptoms with any activity

48. Treatment by Functional Class Mild Heart Failure: NYHA Class I ACE-Is Moderate Heart Failure: NYHA Class II-III ACE-Is Diuretics �-blockers Consider Digoxin Severe Heart Failure: NYHA Class IV Add spironolactone Refer

49. ACE Inhibitors in HF Decrease morbidity and mortality, including Patients with moderately symptomatic HF Patients with severe HF Asymptomatic patients with EF<40% and patients after MI Titrate to maximum doses or SBP 90 mm Hg Side effects include hypotension, renal insufficiency, and cough If patients get cough stop their ACE-I for 1 week, if cough resolves change to ARB, if little or no change restart ACE-I

50. Angiotensin II Receptor Blockers (ARBs) ELITE II: ARBs = ACE-I in terms of mortality (10%) or cardiac death (8%) RCT of added Valsartan to ACE-I in CHF: No difference in mortality but increased mortality when used with ?-blockers Decreased hospitalization, NNT 23 Consider dual ACE-I/ARB inhibition Don�t use ACE-I, ?-blocker, and ARB together Conclusion- ACE-Is remain the 1st choice ARBs are a reasonable 2nd choice ARBs have same Cr increase (~10%); Don�t cause cough

51. ?-blockers in HF Rationale: CHF is catecholamine mediated ?-blockers Improve LVEF, and decrease mortality (~60%), progression, hospitalization, and need for other CHF meds Add to ACE-I and diuretics in compensated CHF (no edema or rales) Carvedilol, bisoprolol, and metoprolol-XL have been studied �Start low, go slow:� double dose every 2 weeks as tolerated May need to increase diuretics temporarily Uncertain if this is a class effect. E.g., bucindolol, a non-selective b-blocker, was not effective.Uncertain if this is a class effect. E.g., bucindolol, a non-selective b-blocker, was not effective.

52. Carvedilol RCT RPCT: 2289 NYHA Class 2-3 patients EF<25% Clinically euvolemic and stable Few rales and little pretibial edema Mean age 63; excluded if K, H, MI, CABG 3.125?25 bid; more withdrew from placebo Cumulative risk of death at 1 year Total population: 11.4% vs 18.5% NNT 14

53. Carvedilol RCT

54. Digoxin in HF No difference in mortality: serum level 1.0-2.0 DIG trial Digoxin decreases hospitalizations for CHF DIG trial Digoxin withdrawal results in worsening symptoms and exercise tolerance despite ACEIs RADIANCE Trial; PROVED Trial

55. Spironolactone in HF Aldosterone increases sodium and water retention RALES trial: RPCT of 1663 patients, EF < 35% and class IV (or class III) HF Excluded patients with Cr > 2.5 or K > 5 mmol/L Almost all patients were on diuretics and ACE-I, only 10% were on ?-blocker 12.5 - 25 mg spironolactone vs. placebo Now a 2nd trial by Pitt et al in NEJM 2003 using another aldosterone receptor blocker in postMI patients with low EF.Now a 2nd trial by Pitt et al in NEJM 2003 using another aldosterone receptor blocker in postMI patients with low EF.

56. Spironolactone in HF Discontinued early: 30% risk reduction for mortality Absolute risk reduction for mortality at 24 months was 9% (NNT = 11) Fewer hospitalizations, significant symptom relief Side effects: gynecomastia in 10%, no difference in serious hyperkalemia Conclusion: consider use in patients with severe HF, once ACE-I and diuretics are optimized. What about ?-blockers?? Hyperkalemia and renal insufficiency have been greater issues in clinical use than in the trial Another study by Pitt, et al. NEJM 2003: eplerenone in patients Post-MI with reduced EF.Another study by Pitt, et al. NEJM 2003: eplerenone in patients Post-MI with reduced EF.

57. Other HF Treatment Tips Diuretics: use a loop diuretic in all patients with volume overload Dose QD until high dose, e.g.> 160 mg furosemide Patients who can�t tolerate ACEIs/ARBs Hydralazine and isosorbide dinitrate Anticoagulation: All patients with ischemic HF should be on ASA (or other antiplatelet agent) Consider warfarin in patients with EF < 25% (poor data) First afterload reduction trial (VeHEFT I) used ISDN and hydralazine. Really have to push the hydralazine dose.First afterload reduction trial (VeHEFT I) used ISDN and hydralazine. Really have to push the hydralazine dose.

58. Treatment of arrhythmias Sudden death is a major cause of death in patients with CHF In general, treat medically only if symptomatic � antiarrhythmics tend to be proarrhythmic Amiodarone: conflicting trials meta-analysis suggests ~ 3% absolute decrease in arrhythmic/sudden death Increasing interest in using ICDs, but cost is a major issue (about $20k per device)Increasing interest in using ICDs, but cost is a major issue (about $20k per device)

59. Treatment of arrhythmias: Device Therapy MADIT II: post-MI with EF < 30% (severe HF) randomized to ICD vs. usual medical therapy 5.6% absolute decrease in mortality at 20 months (NNT = 18) ICDs approved for patients with ischemic cardiomyopathy and EF < 30% Several smaller studies suggest that ICDs reduce sudden death in patients with non-ischemic dilated cardiomyopathy (EF = 30%) with syncope or documented VF Increasing interest in using ICDs, but cost is a major issue (about $20k per device)Increasing interest in using ICDs, but cost is a major issue (about $20k per device)

60. Case 3 An 80 y.o. man is rushed to the emergency room by paramedics with acute respiratory distress. On exam, he appears short of breath. R 34, BP 130/90, P 167 and irregularly irregular. You listen to his lungs and there are absent breath sounds at the bases with crackles to the apices. What is the problem and what would you do initially? How will you manage him after his acute symptoms are controlled? CHF due to AF with RVR --- slow him down, consider cardioversion.CHF due to AF with RVR --- slow him down, consider cardioversion.

61. Case 3 An 80 y.o. man is rushed to the emergency room by paramedics with acute respiratory distress. On exam, he appears short of breath. R 34, BP 130/90, P 167 and irregularly irregular. You listen to his lungs and there are absent breath sounds at the bases with crackles to the apices. Slow rate now: shock vs. metoprolol or dilitiazem Rate control, assess LV function, diuretics & other Rx as needed CHF due to AF with RVR --- slow him down, consider cardioversion.CHF due to AF with RVR --- slow him down, consider cardioversion.

62. Case 4 A 78 yo man presents to the hospital with dyspnea on exertion. He is a former smoker and had a 3V CABG 8 years ago. He has chronic stable angina. His meds include aspirin, metoprolol, simvastatin, ipratropium bromide, and albuterol. BP is 156/95; P = 118 & regular, T = 37, RR 35. He has diffuse coarse crackles. His heart sounds are distant, but no S3 is appreciated. You and your resident disagree over whether the JVP is elevated. He has no peripheral edema. What is your differential? What tests would be helpful? Check BNP � COPD vs. CHFCheck BNP � COPD vs. CHF

63. BNP and the diagnosis of HF BNP is released from both ventricles in response to volume or pressure overload It acts as a vasodilator Breathing Not Properly study (BNP) 1538 pts who presented to ERs with dyspnea Clinical estimate of probability of CHF BNP assay Gold standard = chart review by cardiologists

64. BNP and the diagnosis of HF BNP > 100 pg/mL was more accurate for the diagnosis of CHF than clinical judgment by ER attendings Clinicians were very good at designating �high clinical probability� of CHF BNP was a useful adjunct to clinical diagnosis in �intermediate clinical probability� of CHF Levels of BNP higher than 150 pg/mL are more specific for CHF, but false positives occur BNP should not supplant clinical evaluation (or echocardiography)

65. Case 5 A 60 y.o. man with a history of mild renal insufficiency, Cr 1.7, comes to your office complaining he has to sleep in a chair because of shortness of breath. For months he has had to get up to go to the window several times a night. He also complains of worsening low back pain. On exam: BP 150/70, P 97 reg., RR 26, T 37.0. He has an S4, JVP of 10 cm, and 2+ pitting edema. Labs are remarkable for a Cr = 3.6, and Ca 2+ of 10.5 with an albumin of 2.5. LS spine films show collapse of T10 with several punched out lesions in other vertebral bodies. What is the diagnosis & can it explain his CHF? Myeloma � cardiac amyloidosis (infiltrative/restrictive)Myeloma � cardiac amyloidosis (infiltrative/restrictive)

66. HF with Preserved EF 30-50% of patients with HF Suspect in patients with chronic HTN, elderly (women), diabetes, + S4, LVH on ECG, HTN with CHF exacerbation, symptoms in excess of cardiac silhouette on CXR Causes: hypertension, diabetes, HOCM, or infiltration Common in the elderly (women > men) Diagnosis: Echocardiogram BNP may be helpful in symptomatic patients No true gold standard for diagnosis

67. HF with Preserved EF Treatment: Lower BP & slow rate (improved diastolic filling) Treat ischemia when possible �-Blockers (1st choice), verapamil or diltiazem (no evidence for increased survival), ACE-I/ARB Exercise training Beware overdiuresis ? decreased LV filling Treat other cardiovascular risk

68. Case 7 A 50 y.o. man comes to your office with his wife who says that his snoring keeps her awake. She worries because stops breathing for several seconds at a time while he is asleep. He feels he sleeps fine but he feels sleepy in the afternoon and can�t seem to stay awake. He also has morning headaches. PE reveals an obese man with BP 150/90, BMI 32. HEENT is normal. CV: RRR S1,S2, S3. Chest: clear. Ext: 3+ pitting edema to the knees. EKG shows RVH and frequent PVC�s. CXR shows an enlarged heart and no lung edema. What kind of heart failure is this? Cor pulmonale (right-sided HF) due to obstructive sleep apnea.Cor pulmonale (right-sided HF) due to obstructive sleep apnea.

69. HF Take Home Message Use your history and physical examination DOE, orthopnea, JVP, S3, PMI > 3 cm, AJR Echocardiogram is confirmatory Classify by NYHA Systolic versus diastolic Consider other etiologies if cause is not obvious Treat all patients with systolic dysfunction with ACE-Is Add �-blockers if possible Use diuretics for volume overload